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Leptin and Refeeding
By NG (http://www.theministryoffitness.com/)
You can think of leptin as sort of a master controller of metabolism (along with many others systems). Released primarily from fat cells, leptin has both central (in the brain) and peripheral (in tissues such as muscle and fat cells) effects.
Centrally, among other things, leptin controls hormones like NPY (involved very heavily in appetite regulation), thyroid stimulating hormone, leutinizing hormone and follicular stimulating hormone, growth hormone releasing hormone, and corticotropin releasing hormone (I'm probably forgetting something).
At least it does all of this reliably in rat models, there is some debate as to whether leptin controls every system as much in humans (esp. the GH loop). (Ed: GH = Growth Hormone)
Leptin levels are determined primarily by bodyfat percentage (with other effects from distribution, i.e. gynoid vs. android patterns and sub-q vs. visceral patterns, women also typically have three times the leptin levels as men given the same bodyfat percentage) and is heavily determined by caloric flux (more accurately, caloric flux through the fat cell).
Researchers have identified a system that 'senses' nutrient flux (flux = what's going in versus what's going out) through both fat and muscle cells. This affects a lot of process. When dieting, more calories are leaving the fat cell than are going in (negative flux). This nutrient sensing system 'senses' this and affects many processes, one of which is leptin production (decreasing leptin production).
So leptin drops.
When overfeeding, more calories are entering the fat cells than are leaving (positive flux). The system 'senses' this and affects many processes, one of which is leptin production (increasing leptin production).
So leptin increases.
Hence the need for cyclical dieting (which Elzi has expounded on at great length): when dieting, leptin drops and your body fights back.
By refeeding, leptin can increase again and reverse some of the negative adaptations, so that you can lose fat more easily when you cut calories again.
Leptin goes up as fat mass increases and goes down as fat mass decreases, it goes up when you overfeed, and down when you underfeed (note: the increase/decrease happens a lot more quickly than would be predicted by changes solely in fat mass).
When leptin goes down (during caloric restriction/fat loss), you get an increase in NPY (increasing appetite, especially for carbs), a decrease in TSH, a decrease in GHRH, a decrease in LH/FSH, and an increase in CRH. So thyroid drops, GH drops, testosterone/estrogen drop, cortisol goes up (to what extent this occurs depends on a lot of factors such as starting bodyfat percentage, caloric deficit, length of the deficit, etc, etc ; a lean individual will suffer these effects to a greater degree than an obese individual on account of the obese individual having a higher baseline leptin level but that gets into issues of receptor saturation and stuff).
Basically, the negative hormonal effects of dieting seem to be regulated to a great degree by leptin (there are other feedback loops operating of course). At the very least, the leptin system appears to coordinate the adaptations to dieting that occur (that cause the problems). Random note: leptin also appears to 'turn on' all the good hormonal effects that occur during puberty (i.e. it coordinates all of the anabolic hormonal effects that occur), and is a big part of exercise/caloric restriction induced ammenorrhea in women.
Peripherally, leptin is involved in things such as fat burning, glycogen storage, and plays a role in immune system function. There are other effects such as inside the fat cell lipolysis and even fat cell deletion that have been shown to occur in rats but it's at levels of leptin that are basically impossible without injection in lean humans.
As leptin drops, fat burning and mobilization becomes more difficult (both through direct effects of leptin, as well as changes in hormone levels) which is part of why you lose more muscle as you get leaner. Leptin also plays a role in insulin sensitivity/resistance. It also potentiates the appetite blunting effects of CCK (cholecystokinin). Etc, etc, etc.
It won't surprise me if research finds that leptin has an effect on just about every system in the body, which makes some sort of evolutionary sense. Leptin production and levels (along with sensitivity of course) essentially 'tell' your brain how many calories you're eating and how much you have stored, which determines to a great degree what it can't and can't do. [1]
Refeeding?
When they (Ed: plasma leptin levels) decline to a certain concentration, appetite increases considerably. This is also associated with a gradual shift in many mechanisms (both centrally and peripherally) that induce what is known as the dreaded plateau: decrease in SNS activity, slow down of the metabolism, suppression of the immune system, etc. Ideally, you want to prevent that downward spiral before the plateau establishes. But we can't do that without blood analysis. So, as soon as you start feeling a voracious appetite, then do either a full day of refeeding at above maintenance with carbs, low fat (try to derive most of your dietary fat from essential fatty acids, a balance of o-6 and 0-3s). Or eat a eucaloric diet (maintenance calories) for 2-3 days.
The issue is trying to repay much of the energy deficit, to reset leptin levels (they won't return to baseline, but they should discontinue plummeting) and the SNS activity. The leaner you are, the less fat mass you have, the less leptin you secrete and the more difficult it is to keep leptin levels within an operative threshold. If you are really lean, you may have to refeed every 4 days. And make ensure you intake plenty of zinc.
Also, you want to avoid a suppressed BMR. Which is why periodic refeeding, such as in the CKD (Ed: Cyclical Ketogenic Diet), is beneficial. The study demonstrated that when overfeeding (130% TEE) for 3 days, even if the excess in energy intake was stored as bodyfat, the change in fat would only be 0.3 kg, which is less than 2% of the baseline bodyfat. Imagine what would happen to that if the study subjects were exercising. [2]
What's the importance of all of this?
Incorporate refeeding into your dieting to stop Leptin levels from plummeting (for reasons illustrated above).
By NG (http://www.theministryoffitness.com/)
You can think of leptin as sort of a master controller of metabolism (along with many others systems). Released primarily from fat cells, leptin has both central (in the brain) and peripheral (in tissues such as muscle and fat cells) effects.
Centrally, among other things, leptin controls hormones like NPY (involved very heavily in appetite regulation), thyroid stimulating hormone, leutinizing hormone and follicular stimulating hormone, growth hormone releasing hormone, and corticotropin releasing hormone (I'm probably forgetting something).
At least it does all of this reliably in rat models, there is some debate as to whether leptin controls every system as much in humans (esp. the GH loop). (Ed: GH = Growth Hormone)
Leptin levels are determined primarily by bodyfat percentage (with other effects from distribution, i.e. gynoid vs. android patterns and sub-q vs. visceral patterns, women also typically have three times the leptin levels as men given the same bodyfat percentage) and is heavily determined by caloric flux (more accurately, caloric flux through the fat cell).
Researchers have identified a system that 'senses' nutrient flux (flux = what's going in versus what's going out) through both fat and muscle cells. This affects a lot of process. When dieting, more calories are leaving the fat cell than are going in (negative flux). This nutrient sensing system 'senses' this and affects many processes, one of which is leptin production (decreasing leptin production).
So leptin drops.
When overfeeding, more calories are entering the fat cells than are leaving (positive flux). The system 'senses' this and affects many processes, one of which is leptin production (increasing leptin production).
So leptin increases.
Hence the need for cyclical dieting (which Elzi has expounded on at great length): when dieting, leptin drops and your body fights back.
By refeeding, leptin can increase again and reverse some of the negative adaptations, so that you can lose fat more easily when you cut calories again.
Leptin goes up as fat mass increases and goes down as fat mass decreases, it goes up when you overfeed, and down when you underfeed (note: the increase/decrease happens a lot more quickly than would be predicted by changes solely in fat mass).
When leptin goes down (during caloric restriction/fat loss), you get an increase in NPY (increasing appetite, especially for carbs), a decrease in TSH, a decrease in GHRH, a decrease in LH/FSH, and an increase in CRH. So thyroid drops, GH drops, testosterone/estrogen drop, cortisol goes up (to what extent this occurs depends on a lot of factors such as starting bodyfat percentage, caloric deficit, length of the deficit, etc, etc ; a lean individual will suffer these effects to a greater degree than an obese individual on account of the obese individual having a higher baseline leptin level but that gets into issues of receptor saturation and stuff).
Basically, the negative hormonal effects of dieting seem to be regulated to a great degree by leptin (there are other feedback loops operating of course). At the very least, the leptin system appears to coordinate the adaptations to dieting that occur (that cause the problems). Random note: leptin also appears to 'turn on' all the good hormonal effects that occur during puberty (i.e. it coordinates all of the anabolic hormonal effects that occur), and is a big part of exercise/caloric restriction induced ammenorrhea in women.
Peripherally, leptin is involved in things such as fat burning, glycogen storage, and plays a role in immune system function. There are other effects such as inside the fat cell lipolysis and even fat cell deletion that have been shown to occur in rats but it's at levels of leptin that are basically impossible without injection in lean humans.
As leptin drops, fat burning and mobilization becomes more difficult (both through direct effects of leptin, as well as changes in hormone levels) which is part of why you lose more muscle as you get leaner. Leptin also plays a role in insulin sensitivity/resistance. It also potentiates the appetite blunting effects of CCK (cholecystokinin). Etc, etc, etc.
It won't surprise me if research finds that leptin has an effect on just about every system in the body, which makes some sort of evolutionary sense. Leptin production and levels (along with sensitivity of course) essentially 'tell' your brain how many calories you're eating and how much you have stored, which determines to a great degree what it can't and can't do. [1]
Refeeding?
When they (Ed: plasma leptin levels) decline to a certain concentration, appetite increases considerably. This is also associated with a gradual shift in many mechanisms (both centrally and peripherally) that induce what is known as the dreaded plateau: decrease in SNS activity, slow down of the metabolism, suppression of the immune system, etc. Ideally, you want to prevent that downward spiral before the plateau establishes. But we can't do that without blood analysis. So, as soon as you start feeling a voracious appetite, then do either a full day of refeeding at above maintenance with carbs, low fat (try to derive most of your dietary fat from essential fatty acids, a balance of o-6 and 0-3s). Or eat a eucaloric diet (maintenance calories) for 2-3 days.
The issue is trying to repay much of the energy deficit, to reset leptin levels (they won't return to baseline, but they should discontinue plummeting) and the SNS activity. The leaner you are, the less fat mass you have, the less leptin you secrete and the more difficult it is to keep leptin levels within an operative threshold. If you are really lean, you may have to refeed every 4 days. And make ensure you intake plenty of zinc.
Also, you want to avoid a suppressed BMR. Which is why periodic refeeding, such as in the CKD (Ed: Cyclical Ketogenic Diet), is beneficial. The study demonstrated that when overfeeding (130% TEE) for 3 days, even if the excess in energy intake was stored as bodyfat, the change in fat would only be 0.3 kg, which is less than 2% of the baseline bodyfat. Imagine what would happen to that if the study subjects were exercising. [2]
What's the importance of all of this?
Incorporate refeeding into your dieting to stop Leptin levels from plummeting (for reasons illustrated above).
